Gastrointestinal Tract Diseases Overview

Gastrointestinal Tract (GIT) Diseases

• Oral Cavity:

  • Aphthous ulcers: Painful, superficial ulcers of unknown cause; may be associated with systemic diseases.
  • Herpes simplex virus (HSV): Causes a self-limited infection with vesicles (cold sores); latent virus in nerve ganglia can reactivate.
  • Oral candidiasis: Occurs when the oral microbiota is altered, e.g., after antibiotic use; immunosuppressed individuals at risk for invasive disease.
  • Fibromas and pyogenic granulomas: Common reactive lesions of the oral mucosa.
  • Leukoplakia: White, well-defined mucosal patch/plaque; caused by epithelial thickening/hyperkeratosis; common in older individuals (lower lip, buccal mucosa, hard/soft palate); can progress to carcinoma in situ; Risk factors include tobacco, chronic friction, alcohol, irritants, HPV.
  • Oral cancers: Mostly squamous cell carcinomas; Risk factors include leukoplakia, erythroplasia, tobacco, alcohol, HPV types 16, 18, and 11, chronic irritation, Plummer-Vinson syndrome; Common sites include lateral margins of lower lip, floor of mouth, lateral borders of tongue.

• Salivary Gland Diseases:

  • Sialadenitis: Inflammation of salivary glands, caused by trauma, infection (e.g., mumps), or autoimmune reaction.
  • Pleomorphic adenoma: Slow-growing benign neoplasm; heterogeneous mixture of epithelial/mesenchymal cells.
  • Mucoepidermoid carcinoma: Malignant neoplasm of variable aggressiveness; mixture of squamous/mucous cells.
  • Salivary gland tumors: 80% in parotid glands; equal male/female ratio; (6th/7th decades of life); 70-80% of parotid tumors are benign; Pleomorphic adenomas are slow-growing, well-demarcated, encapsulated tumors; rarely exceed 6 cm in diameter; Histologically: epithelial elements from ducts, acini, tubules, strands or sheets of cells; loose myxoid connective tissue stroma; chondroid or bone.

• Diseases of the Esophagus:

  • Hiatal hernia: Two types: Sliding hernia (95%) and rolling (paraeosophageal) hernia; common presentation is reflux esophagitis.
  • Achalasia: Incomplete relaxation of lower esophageal sphincter (LES) upon swallowing; obstruction of lower esophagus, dilatation of proximal part; Classic secondary example is Chagas disease (T. cruzi); risk for squamous cell carcinoma in 5% of cases.
  • Barrett's esophagus: Complication of long-standing esophageal reflux (11% of symptomatic patients); replacement of normal distal squamous epithelium by abnormal metaplastic columnar epithelium containing goblet cells. High risk of adenocarcinoma (30-40x).
  • Esophagitis: Causes include prolonged gastric intubation, uremia, ingestion of corrosives/irritants, radiation, chemotherapy, and reflux. Microscopically: Eosinophils/neutrophils; basal zone hyperplasia; lamina propria papillae elongation. Complications include bleeding, strictures, Barrett's metaplasia leading to cancer.
  • Esophageal carcinoma: Mostly squamous cell carcinoma or adenocarcinoma; male/female ratio of 3:1; Risk factors include long-standing esophagitis, achalasia, Plummer-Vinson syndrome, alcohol/tobacco, vitamin/trace mineral deficiencies, nitrosamines. Squamous cell carcinomas arise from squamous dysplasia or carcinoma in situ as small grey-white plaque-like thickenings. Tumour types: Polypoid fungating masses, necrotizing ulcerations, diffuse infiltration; (20% cervical/upper thoracic, 50% middle third, 30% lower third). Adenocarcinoma (25% of esophageal cancers), usually in the lower esophagus.

• Diseases of the Stomach:

  • Chronic gastritis: Mucosal inflammatory changes leading to mucosal atrophy and epithelial metaplasia. Pathogenesis: H. pylori (most important pathogen); autoimmune (autoantibodies against gastric parietal cells); unknown causes (mostly Japan). H. pylori infection → antral gastritis. Over time can lead to pangastritis and risk for multifocal atrophic gastritis. Autoimmune type is often seen with other autoimmune disorders.
  • Acute gastritis: Acute inflammation (transient), accompanied by hemorrhage and sloughing of superficial mucosa (erosion); Heavy NSAID use, alcohol, smoking, chemo, uremia, systemic infection (e.g., typhoid), severe stress (trauma, burns, surgery), ischemia/shock, ingestion of acids/alkalis, mechanical trauma (N.G. tube), bile reflux after partial gastrectomy. Pathophysiology: Disruption of mucosa, acid secretion stimulation, decreased bicarbonate production, reduced mucosal blood flow, direct damage of epithelium. Microscopically: Superficial to complete mucosal involvement; mucosal edema, neutrophilic infiltrate, chronic inflammatory infiltrate, and regenerative replication.
  • Peptic ulceration: Mucosal breach extending to or through muscularis mucosae; 98% in duodenum (first portion). More frequent in alcoholic cirrhosis, COPD, chronic renal failure, hyperparathyroidism (hypercalcemia increases gastrin). Pathogenesis: Imbalance between mucosal defense (mucus, bicarbonate, mucosal blood flow, apical transport, epithelial regeneration, prostaglandins) vs. aggressive forces (gastric acidity, H. pylori). H. pylori in 100% of duodenal ulcers and 70% gastric ulcers; signs of H.pylori pathogenesis include urease secretion, proteases, phospholipases, neutrophil production, and thrombotic occlusion. Grossly: Rounded, sharply punched-out crater (2-4 cm), in duodenum (anterior/posterior walls), lesser curvature of stomach; margins punched out without significant edge elevations. Histologically: 4 zones- base/margins, active inflammatory cells (mostly neutrophils), granulation tissue, fibrous scar. -Acute ulceration (severe stress): severe trauma, burns (Curling's), CNS injury (Cushing's), chronic NSAID/corticosteroid use. -Gastric carcinomas: 90-95% carcinomas, 4% lymphomas, 3% carcinoids, 2% GISTs. Two types: Intestinal (on intestinal metaplasia, M:F ratio 2:1), Diffuse (in younger patients, M:F ratio 1:1). Intestinal type pathogenesis: diet (nitrites, smoked food, pickles, excess salt, decreased fresh vegetables), H. pylori infection, pernicious anemia, altered anatomy (subtotal gastrectomy). Diffuse type pathogenesis: unknown. Pylorus & antrum (50-60%), cardia (25%), body & fundus (15-25%), lesser curvature (40%), greater curvature (12%). Macroscopically: Exophytic, flat/depressed, excavated, linitis plastica (diffuse thickening/permeation of gastric wall).

• Small and Large Intestines:

  • Meckel's diverticulum: Failure of omphalo-mesenteric duct involution; blind-ended tubular protrusion; partial intestine layers.
  • Hirschsprung's disease: Dilated colon (>6-7 cm); functional obstruction due to absent Meissner's/Auerbach's plexuses; male/female ratio 4:1;
  • Acquired megacolon: Chagas disease, organic obstruction, toxic megacolon (UC/CD), functional obstruction.
  • Ischemic bowel disease: Arterial thrombosis (severe atherosclerosis, systemic vasculitis), embolism, venous thrombosis (oral contraceptives, antithrombin III deficiency), non-occlusive ischemia (HF, shock), radiation, volvulus, hernias. Three histological types: Transmural, mural, mucosal.
  • Angiodysplasia: Tortuous dilation of submucosal/mucosal blood vessels; cecum/right colon; after 6th decade; 20% lower intestinal bleeding.
  • Diarrheal diseases: Secretory, osmotic, exudative (infectious, IBD), malabsorption, motility disorders.
  • Malabsorption syndromes: Defective intraluminal digestion, terminal digestion, transepithelial transport; causes include pancreatic insufficiency, Zollinger-Ellison syndrome, ileal dysfunction/resection, biliary obstruction/hepatic dysfunction, lactase deficiency, bacterial overgrowth, abetalipoproteinemia, celiac disease, short gut syndrome, Crohn's disease, and lymphatic obstruction.
  • Celiac disease (gluten-sensitive enteropathy): Sensitivity to gluten in wheat, oats, barley, rye; gliadin proteins; flattened mucosal villi.
  • Idiopathic inflammatory bowel diseases (Crohn's disease, ulcerative colitis): Idiopathic; Genetic predisposition; abnormal intestinal structure; infectious causes; abnormal immune reactivity.
  • Crohn's disease: Granulomatous; affects any part of the GI tract; transmural involvement; neutrophilic infiltration; crypt abscess; often skip lesions; can be associated with iritis, uveitis, etc.; small intestine involvement (40%), small/colon (30%), colon alone (30%).
  • Ulcerative colitis: Nongranulomatous ulcero-inflammatory affecting colon; limited to mucosa/submucosa; starts in rectum, extends proximally; associated with other issues; common in western countries. Transmural involvement (diffuse mononuclear infiltrate, crypt abscess); associated with architectural disarray and fibrosis.
  • Familial polyposis syndrome: Autosomal dominant; development of 500-2500 colonic adenomas (tubular); risk of colon cancer is high; diagnosed with 100+ detected polyps.
  • Colorectal carcinomas: 98% adenocarcinomas; arise on adenomatous polyps; peak incidence 60-70 yrs; M:F ratio (20% more males); associated with high-refined carbohydrates, low-fiber diets, etc. (CECUM/ASCENDING COLON, RECTUM, DESCENDING/SIGMOID, SCATTERED); 1-3% occur in FAP or IBD patients.
  • Anal cancers: Squamous cell carcinomas.
  • Carcinoid tumors: Neuroendocrine tumors; from various GI sites; tendency to be aggressive correlates with site, depth & size.

Blood Vessels

• Endothelial cell function: Permeability barrier maintenance, anticoagulation/antithrombosis/fibrinolysis regulation (prostacyclin, thrombomodulin, heparin-like molecules, plasminogen activator), prothrombotic molecule elaboration (von Willebrand factor, tissue factor, plasminogen activator inhibitor), ECM production, blood flow modulation, inflammation and immunity regulation, cell growth regulation, LDL oxidation. Activated by cytokines, bacterial products, hemodynamic stresses, lipids, diabetes, viruses, complements, & hypoxia.
• Vascular smooth muscle cells: Vasoconstriction/dilation, synthesize collagen, elastin, proteoglycans; elaborate growth factors/cytokines; migrate/proliferate following injury. Vascular structure/function tightly regulated in basal & activated states; physiologic/pathophysiologic stimuli can induce activation/dysfunction.
• Atherosclerosis: Intimal lesions (atheromas); cause of ischemic heart disease; American Heart Association classifies into six types; caused by vessel wall injury/inflammation; can result in stable vs vulnerable plaques. Fatty streaks are earliest lesions; composed of subendothelial lipid-filled foam cells. Complications include rupture, ulceration, hemorrhage, thrombosis, aneurysm. Risk factors: Aging, male gender, family history, genetics, hyperlipidemia, hypertension, smoking, diabetes, obesity, inactivity, stress, postmenopausal estrogen deficiency, high carbohydrate intake, alcohol. Pathogenesis: endothelial injury, lipoprotein accumulation, lipoprotein oxidation, monocyte migration, platelet adhesion, smooth muscle cell migration/proliferation, lipid accumulation.
• Hypertension: Common disorder affecting 25% of the population, major risk factor for atherosclerosis, heart failure, renal failure. Can be essential (95%) or secondary. Pathogenesis is complex, multifactorial. Types include Essential & Secondary. Secondary includes renal, endocrine (e.g., Cushing syndrome, hyperaldosteronism, pheochromocytoma), pregnancy-induced, cardiovascular, neurologic, sleep apnea. Kidneys regulate blood pressure via renin-angiotensin system, prostaglandins/NO, sodium conservation.
• Vasculitis: Inflammation of vessel walls; often systemic manifestations & organ dysfunction; can be infectious or immune-mediated (immune complex deposition, ANCA/anti-endothelial cell antibodies), specific vessel types.
  • Variants: Giant cell arteritis, Takayasu's arteritis, polyarteritis nodosa, Kawasaki disease, microscopic polyangiitis, Wegener's granulomatosis, thromboangiitis obliterans.
• Vascular tumors: Typically benign (e.g., hemangiomas) or highly malignant (e.g., angiosarcoma). Vascular ectasias are not tumors but dilations.

Other Cardiovascular Diseases

• Congenital cardiac diseases: Ventricular septal defect (VSD), atrial septal defect (ASD), pulmonary stenosis, patent ductus arteriosus (PDA), tetralogy of Fallot (TOF), coarctation of aorta, atrioventricular septal defect (AVSD), aortic stenosis, transposition of great arteries (TGA), truncus arteriosus (TA), total anomalous pulmonary venous connection (TAPVC), tricuspid atresia. Proportions for each disease listed in percentage.
• Ischemic Heart Disease (IHD): Diminished coronary perfusion relative to myocardial demand; fixed atherosclerotic narrowing, intraluminal thrombosis, platelet aggregation, vasospasm. Obstruction leads to exertion symptoms, and 90% leads to rest symptoms (angina); acute plaque change can cause myocardial infarction (MI); Acute plaque changes include rupture/fissuring, erosion/ulceration, hemorrhage. Morphological effects vary based on time from initial injury.
  • Consequences of MI: Contractile dysfunction; arrhythmias; myocardial rupture; pericarditis; infarct extension; infarct expansion; mural thrombus; ventricular aneurysm; papillary muscle dysfunction; progressive late heart failure.
• Infective Endocarditis (IE): Heart valve or mural endocardium colonization; destruction of tissues often; friable vegetations (thrombotic debris & organisms); classified as acute or subacute; can be caused by various microbes (Streptococcus viridans, Staphylococcus aureus, others).
• Rheumatic Heart Disease (RHD): Immunologically mediated multisystem inflammatory disease, few weeks after group A streptococcal pharyngitis; acute rheumatic carditis can progress; focal inflammatory lesions in tissues (Aschoff bodies, composed of swollen eosinophilic collagen surrounded by lymphocytes, plasma cells, plump macrophages (Anitschkow cells)); can affect all heart layers; chronic damage leads to valvular thickening and retraction.
  • Cardinal anatomic changes of the mitral/tricuspid valves: leaflet thickening, commissural fusion, and shortening of tendinous cords.
• Varicose veins: Deep/superficial vein dilatation; role of valves, muscle pump, blood volume/position. Symptoms include cosmetic concerns, pain, inflammation, leg ulcer, and rupture. Diagnosis: inspection, Doppler ultrasound, and duplex ultrasound. Etiology is related to congenital weakness/absence of valves; Genetic, gender, age, ethnic, body mass index, family history, lifestyle, and Pregnancy impact. Deep vein incompetency (retrograde flow) may have complications.
• Aneurysm & Dissections: Aneurysm is weakened/destroyed arterial wall dilation or balloon-like bulge (Congenital/acquired dilation involving entire wall). Complications: rupture/thrombosis/embolization. Dissections are blood entering vessel wall separating layers leading complications. Common location: Thoracic & abdominal aorta; Cerebral; Peripheral. Types: (Aortic (abdominal/thoracic), Cerebral, Peripheral).
• Heart failure: Inability to meet metabolic needs; systolic/diastolic dysfunction; compensatory mechanisms (Frank-Starling mechanism, ventricular remodeling, neurohormonal systems) lead to a vicious cycle; common etiologies include ischemic heart disease, hypertension, diabetes. Different types of LV failure, RV failure, sequels, and pathophysiology are outlined.

Test your knowledge on various diseases of the gastrointestinal tract, focusing on the oral cavity. This quiz covers conditions like aphthous ulcers, herpes simplex virus, oral candidiasis, and oral cancers. Learn about their causes, risk factors, and implications for health.